Interaction of cerebral hemodynamics and metabolism

Abstract

Normal values of cortical tissue pO2 varied between 10 and 20 mm Hg with the animal breathing air. pCO2 readings from the same area varied between 23 and 68 mm Hg, depending on respiratory exchange. pH values varied between 7.0 and 7.5 units. Certain changes in electroencephalographic activity (activation with stroboscopic stimulation, strychnine application, and arousal reaction) resulted in decreased cortical pO2 and increased pCO2 followed by cortical hy- peremia, which tended to restore pO2 and pCO2 levels toward normal. Seizures induced by strychnine decreased cortical pO2 and pH but increased the cortical pCO2 with resulting hyperemia. When the seizures were inhibited by ischemia, the inhibitory effect was due primarily to anoxia rather than increased pCO2. During nitrogen breathing, cerebral vasodilation was due to anoxia, since reduction of cortical oxygen tension was unaccompanied by a rise in pCO2. Decreased cortical activity due to cyanide, barbiturates, drowsiness, or ischemic anoxia resulted in an increase in tissue pO2 and a fall in brain pCO2. Inhalation of carbon dioxide or the intravenous injection of sodium bicarbonate or "carbonic acid" produced increased cortical blood flow. The intravenous injection of acetazoleamide resulted in a rise in brain pCO2 and inhibited the vasodilator effects of carbon dioxide, sodium bicarbonate, and "carbonic acid." Increased pCO2 in the blood or diffusion to the cerebral vessels from brain tissue caused vasodilation, but carbonic anhydrase appeared necessary to produce the vasodilator effect. Cerebral venous occlusion resulted in a fall in brain pO2 and a rise in brain pCO2. Cerebral arterial occlusion resulted in a fall in brain pO2 and a rise in brain pCO2 in the territory of supply. These changes stimulated the collateral blood flow. If cortical pO2 fell to near zero levels, electro-encephalographic slowing and reduced cortical metabolism resulted, with lowered pCO2 and increased pO2 levels. If collateral circulation was improved, normal metabolism tended to be restored; if collateral circulation failed, the cortical pO2 fell to zero and cerebral infarction resulted. There appeared to be a nomeostatic mechanism within the brain whereby cerebral metabolism regulated local metabolic requirements. The most important single factor in this mechanism was local CO2 production.